Q-omics provides the consensus-scored PDPN profile across patient tissues and cancer cell-line models. PDPN expression is associated with patient survival in 28 of 34 cancer types, with the highest sampling consensus in HNSC. Among the 18 cancer types available for tumor–normal comparison, PDPN is differentially expressed in 12, with the highest sampling consensus in HNSC. Additionally, PDPN RNA expression shows 18,468 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight HNSC, and LUAD as cancer lineages where PDPN shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for PDPN — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes PDPN survival associations across molecular data types. PDPN RNA expression shows survival associations in the most cancer types (28), followed by mutation status (2) and mass-spec protein abundance (3). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible PDPN RNA expression–survival associations across cancer types. High PDPN expression shows unfavorable associations in HNSC, LGG, ACC and OV, but favorable associations in MESO and DLBC. The HNSC Kaplan–Meier curve shows clear separation, with the high-expression group declining faster, consistent with the unfavorable association (log-rank p = .001). Together, the overview and detailed table identify HNSC as the clearest survival context for PDPN RNA expression.
This table summarizes PDPN tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 12, while mass-spec protein shows differences in 3. The strongest signals are observed in HNSC for RNA and HNSC for protein.
This table ranks reproducible tumor–normal expression differences for PDPN. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. PDPN shows lower tumor expression in LUAD, THCA, UCEC and KIRC and higher tumor expression in HNSC and COAD. The HNSC box plot shows higher PDPN RNA expression in tumor versus normal tissue (log2 FC = +3.390, t-test p < 0.001).
This table shows molecular features associated with PDPN in patient tissues and cancer cell lines. In patient samples, PDPN shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, PDPN RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LARGE_INTESTINE, while CRISPR and shRNA rows add functional-dependency signals in SOFT_TISSUE and BONE.
